MAD2-p31comet axis deficiency reduces cell proliferation, migration and sensitivity of microtubule-interfering agents in glioma
- Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai 200237 (China)
- Department of Neurosurgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000 (China)
- Department of Neurology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001 (China)
Mitotic arrest deficient-like-1 (MAD2, also known as MAD2L1) is thought to be an important spindle assembly checkpoint protein, which ensures accurate chromosome segregation and is closely associated with poor prognosis in many cancer. As a MAD2 binding protein, p31{sup comet} counteracts the function of MAD2 and leads to mitotic checkpoint silence. In this study, we explore the function of MAD2-p31{sup comet} axis in malignant glioma cells. Our results showed that disruption of MAD2-p31{sup comet} axis by MAD2 knockdown or p31{sup comet} overexpression suppressed cell proliferation, survival and migration of glioma, indicating that MAD2-p31{sup comet} axis is required for maintaining glioma cells malignancy. It is noted that MAD2 depletion or p31{sup comet} overexpression reduced the sensitivity of glioma cells to microtubule-interfering agents paclitaxel and vinblastine, providing clinical guidance for application of such drugs. Taken together, our findings suggest that MAD2-p31{sup comet} axis may serve as a potential therapeutic target for glioma.
- OSTI ID:
- 23137260
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 498, Issue 1; Other Information: Copyright (c) 2018 Published by Elsevier Inc.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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